Diabetes insipidus (ED revision)
Diabetes insipidus (DI) is a disorder of water balance caused by deficient antidiuretic hormone (ADH; arginine vasopressin, AVP) secretion (central/cranial DI) or by renal resistance to ADH (nephrogenic DI).
In the emergency department (ED) DI typically presents with large‑volume dilute urine, variable dehydration and disturbances of serum sodium and osmolality.
Rapid recognition and appropriate management are time‑critical: untreated severe DI may cause life‑threatening hypernatraemic dehydration, while unsupervised ADH replacement or uncontrolled free‑water administration can precipitate dangerous hyponatraemia.
This section summarises pathophysiology, causes, ED assessment and investigations, interpretation of fluid‑deprivation testing, and practical management with emphasis on desmopressin safety and post‑neurosurgical DI. See RCEM and MHRA guidance for local policy and reporting requirements.
Physiology in brief
ADH (AVP) is synthesised in the hypothalamus and released from the posterior pituitary in response to increased plasma osmolality or hypovolaemia. ADH acts on V2 receptors in the renal collecting duct to insert aquaporin‑2 channels and concentrate urine.
Loss of ADH (central DI) or renal unresponsiveness to ADH (nephrogenic DI) causes excessive free‑water loss, producing dilute urine and a tendency to hypernatraemia if losses are not replaced.
Key clinical and biochemical features
- Polyuria, often >3 L/24 h; confirm by measurement when possible.
- Very dilute urine with urine osmolality typically <300 mOsm/kg.
- Raised plasma osmolality when uncompensated, typically >300 mOsm/kg.